Quiz: Cell Injury and Protein Metabolism — 12 questions

Detailed questions and answers

1. Which mechanism is recognized as a principal cause of cell injury?

Excessive collagen synthesis
Ischemia and hypoxia
Reduced extracellular calcium
Increased melanin production

Ischemia and hypoxia

Explanation

Ischemia and hypoxia are among the principal mechanisms of cell injury, along with free-radical, toxic, and immune-mediated injury.

2. Which statement correctly distinguishes necrosis from apoptosis?

Necrosis is reversible injury, whereas apoptosis is intracellular protein accumulation
Necrosis affects connective tissue, whereas apoptosis affects functional cells
Necrosis is injury-related cell death, whereas apoptosis is programmed cell death
Necrosis is programmed cell death, whereas apoptosis results from ischemic injury

Necrosis is injury-related cell death, whereas apoptosis is programmed cell death

Explanation

Necrosis is cell death caused by injury, while apoptosis is a form of programmed cell death.

3. Which finding is characteristic of reversible parenchymal change?

Intracellular accumulation of water, proteins, fats, carbohydrates, or pigments
Extracellular deposition of calcium in damaged tissue
Replacement of functional cells by connective tissue
Permanent loss of the cell nucleus with membrane rupture

Intracellular accumulation of water, proteins, fats, carbohydrates, or pigments

Explanation

Reversible parenchymal changes include intracellular accumulation of water, proteins, fats, carbohydrates, and pigments. The defining feature of reversibility is that the cell can recover.

4. Which set contains only forms of intracellular water accumulation?

Hyaline droplets, Russell bodies, and amyloid deposits
Necrosis, apoptosis, and pathological calcification
Cell swelling, hydropic change, and vacuolar change
Fatty infiltration, mucinous change, and fibrinoid swelling

Cell swelling, hydropic change, and vacuolar change

Explanation

Intracellular water accumulation appears as cell swelling, hydropic changes, and vacuolar changes. Hyaline droplets and Russell bodies instead represent protein accumulation.

5. In cell swelling, what do the small cytoplasmic vacuoles represent?

Aggregates of immunoglobulins within plasma-cell nuclei
Lipid droplets formed by fatty infiltration
Deposits of extracellular amyloid in connective tissue
Distended and detached fragments of the endoplasmic reticulum

Distended and detached fragments of the endoplasmic reticulum

Explanation

Cell swelling is a reversible injury in which small cytoplasmic vacuoles represent distended and detached fragments of the endoplasmic reticulum, with loss of fine structures and blurred cell borders.

6. A patient with acute viral hepatitis develops fluid-filled vacuoles in hepatocyte cytoplasm. Which change does this represent?

Vacuolar change
Russell-body formation
Fibrinoid swelling
Hyaline-droplet change

Vacuolar change

Explanation

Vacuolar changes consist of fluid-filled cytoplasmic vacuoles and can occur in the liver during acute viral hepatitis. Hyaline droplets and Russell bodies are protein accumulations.

7. What functional consequence can reversible cell injury produce in an affected organ?

Programmed removal of every injured cell
Reduced organ function, such as impaired myocardial contractility
Increased organ function caused by cellular enlargement
Immediate replacement of the organ by scar tissue

Reduced organ function, such as impaired myocardial contractility

Explanation

Reversible cell injury can reduce organ function; impaired myocardial contractility is an example of this clinical consequence.

8. A patient with nephrotic syndrome has protein droplets filling cells of the proximal convoluted tubules. Which finding best explains this observation?

Cell swelling caused by detached fragments of connective tissue
Russell-body formation caused by immunoglobulin accumulation in plasma cells
Vacuolar change caused by fluid accumulation in hepatocytes
Hyaline-droplet change caused by increased glomerular protein permeability

Hyaline-droplet change caused by increased glomerular protein permeability

Explanation

Hyaline-droplet changes are microscopic protein droplets in proximal convoluted tubules and occur when the glomerular filter becomes more permeable to protein, including in nephrotic syndrome.

9. Which change best defines mesenchymal mucoid edema?

Accumulation of hydrophilic glycosaminoglycans in the interstitial substance with entry of plasma proteins and glycoproteins
Immune-complex injury causing extensive destruction of collagen fibers and entry of fibrinogen
Deposition of insoluble calcium salts within otherwise normal connective tissue
Proliferation of fibroblasts with replacement of ground substance by dense collagen

Accumulation of hydrophilic glycosaminoglycans in the interstitial substance with entry of plasma proteins and glycoproteins

Explanation

Mucoid edema results from the accumulation of hydrophilic glycosaminoglycans in the interstitial substance, accompanied by penetration of plasma proteins and glycoproteins. Marked collagen destruction is characteristic of fibrinoid swelling instead.

10. A connective-tissue ground substance appears reddish rather than blue after toluidine blue staining. Which feature of mucoid edema explains this finding?

Destruction of collagen fibers caused by immune-complex injury
Deposition of fibrinogen within damaged microvessels
Loss of glycosaminoglycans from the interstitial substance
Accumulation of chromotropic substances causing metachromasia

Accumulation of chromotropic substances causing metachromasia

Explanation

Accumulated chromotropic substances make the ground substance metachromatic, so toluidine blue produces a reddish color rather than its usual blue. This staining change reflects the altered glycosaminoglycan-rich matrix.

11. Which mechanism is most characteristic of fibrinoid swelling?

Accumulation of hydrophilic glycosaminoglycans in the ground substance
Binding of hyaluronic acid to plasma proteins without major collagen injury
Immune-complex injury to the microcirculatory bed and connective tissue
Depolymerization of glycosaminoglycans with increased metachromatic staining

Immune-complex injury to the microcirculatory bed and connective tissue

Explanation

Fibrinoid swelling is associated with immune-complex injury involving the microcirculatory bed and connective tissue. Glycosaminoglycan accumulation and related staining changes are characteristic of mucoid edema.

12. What combination of tissue changes is expected in fibrinoid swelling?

Marked collagen destruction with penetration of plasma globulins and fibrinogen
Fibroblast proliferation with replacement of plasma proteins by elastin
Metachromatic ground substance without entry of plasma proteins
Preserved collagen with accumulation of glycosaminoglycans and hyaluronic acid

Marked collagen destruction with penetration of plasma globulins and fibrinogen

Explanation

Fibrinoid swelling involves marked destruction of collagen fibers and penetration of plasma proteins, especially globulins and fibrinogen, into connective tissue. Mucoid edema primarily alters glycosaminoglycans rather than causing major collagen destruction.

Review with flashcards

Memorize the answers with 23 flashcards on Cell Injury and Protein Metabolism.

What are the possible types of cell injury?

Cell injury may be reversible, irreversible, programmed, or residual.

Name some consequences of cell injury.

Consequences include degeneration, necrosis, apoptosis, subcellular injury, intracellular accumulation, gangrene, and pathological calcification.

What are the principal mechanisms of cell injury?

Ischemia and hypoxia, free-radical injury, toxic injury, and immune-mediated injury.

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